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Transient Ischemia (transient + ischemia)
Selected AbstractsAn ultrastructural study of cell death in the CA1 pyramidal field of the hippocapmus in rats submitted to transient global ischemia followed by reperfusionJOURNAL OF ANATOMY, Issue 5 2007Aline De Souza Pagnussat Abstract In the course of ischemia and reperfusion a disruption of release and uptake of excitatory neurotransmitters occurs. This excitotoxicity triggers delayed cell death, a process closely related to mitochondrial physiology and one that shows both apoptotic and necrotic features. The aim of the present study was to use electron microscopy to characterize the cell death of pyramidal cells from the CA1 field of the hippocampus after 10 min of transient global ischemia followed by short reperfusion periods. For this study 25 adult male Wistar rats were used, divided into six groups: 10 min of ischemia, 3, 6, 12 and 24 h of reperfusion and an untouched group. Transient forebrain ischemia was produced using the 4-vessel occlusion method. The pyramidal cells of the CA1 field from rat hippocampus submitted to ischemia exhibited intracellular alterations consistent with a process of degeneration, with varied intensities according to the reperfusion period and bearing both apoptotic and necrotic features. Gradual neuronal and glial modifications allowed for the classification of the degenerative process into three stages: initial, intermediate and final were found. With 3 and 6 h of reperfusion, slight and moderate morphological alterations were seen, such as organelle and cytoplasm edema. Within 12 h of reperfusion, there was an apparent recovery and more ,intact' cells could be identified, while 24 h after the event neuronal damage was more severe and cells with disrupted membranes and cell debris were identified. Necrotic-like neurons were found together with some apoptotic bodies with 24 h of reperfusion. Present results support the view that cell death in the CA1 field of rat hippocampus submitted to 10 min of global transient ischemia and early reperfusion times includes both apoptotic and necrotic features, a process referred to as parapoptosis. [source] The Intracoronary Electrocardiogram in Percutaneous Coronary InterventionJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 1 2009ANDY SC YONG M.B.B.S. The technique of obtaining an epicardial electrocardiogram trace by connecting the guidewire during coronary angioplasty to an electrocardiogram lead has been used since 1985. The intracoronary electrocardiogram appears to be more sensitive than the surface electrocardiogram in detecting transient ischemia, particularly in the territory of the left anterior descending and left circumflex coronary arteries. Importantly, recent studies have shown the intracoronary electrocardiogram to be particularly useful in demonstrating pre- and postconditioning during interventional procedures, predicting periprocedural myocardial damage, and in the determination of regional viability in the catheterization laboratory. Barriers to the use of the intracoronary electrocardiogram in the clinical setting include the lack of standardized methods for acquiring and analyzing the intracoronary electrocardiogram, and the lack of commercially available continuous intracoronary monitoring systems to permit analysis while performing coronary interventions. Facilitating these relatively simple technical developments may permit optimal integration of the intracoronary electrocardiogram into the catheterization laboratory. [source] Increases in tumor necrosis factor-, following transient global cerebral ischemia do not contribute to neuron death in mouse hippocampusJOURNAL OF NEUROCHEMISTRY, Issue 6 2005Yuki Murakami Abstract The actions of tumor necrosis factor-, (TNF-,) produced by resident brain cells and bone marrow-derived cells in brain following a transient global ischemia were evaluated. In wild-type mice (C57Bl/6J) following 20 min ischemia with bilateral common carotid artery occlusion (BCCAo), TNF-, mRNA expression levels in the hippocampus were significantly increased at 3 h and 36 h and exhibited a biphasic expression pattern. There were no hippocampal TNF-, mRNA expression levels at early time points in either wild-type mice bone marrow transplanted (BMT)-chimeric-TNF-, gene-deficient (T/W) or TNF-, gene-deficient mice BMT-TNF-, gene-deficient mice (T/T), although TNF-, mRNA levels were detectable in T/W BMT mice at 36 h. Histopathological findings showed no intergroup differences between wild-type and TNF-, gene-deficient mice at 4 and 7 days after transient ischemia. In addition, nuclear factor-,B (NF-,B) was activated within 12 h after global cerebral ischemia, but electrophoretic mobility shift assays (EMSA) showed no intergroup differences between wild type and TNF-, gene-deficient mice. In summary, early hippocampal TNF-, mRNA expression may not be related to bone marrow-derived cells, and secondary TNF-, expression as early as 36 h after ischemia probably resulted mainly from endogenous brain cells and possibly a few bone marrow-derived cells. Although we cannot exclude the possibility of the TNF-, contribution to the physiologic changes of hippocampus after transient global ischemia, these results indicate that TNF-, does not influence the morphological changes of the hippocampal neurons under our study condition. [source] Endogenously released DOPA is a causal factor for glutamate release and resultant delayed neuronal cell death by transient ischemia in rat striataJOURNAL OF NEUROCHEMISTRY, Issue 3 2001Nobuya Furukawa Glutamate is implicated in neuronal cell death. Exogenously applied DOPA by itself releases neuronal glutamate and causes neuronal cell death in in vitro striatal systems. Herein, we attempt to clarify whether endogenous DOPA is released by 10 min transient ischemia due to four-vessel occlusion during rat striatal microdialysis and, further, whether DOPA, when released, functions to cause glutamate release and resultant delayed neuronal cell death. Ischemia increased extracellular DOPA, dopamine, and glutamate, and elicited neuronal cell death 96 h after ischemic insult. Inhibition of striatal l -aromatic amino acid decarboxylase 10 min before ischemia increased markedly basal DOPA, tripled glutamate release with a tendency of decrease in dopamine release by ischemia, and exaggerated neuronal cell death. Intrastriatal perfusion of 10,30 nm DOPA cyclohexyl ester, a competitive DOPA antagonist, 10 min before ischemia, concentration-dependently decreased glutamate release without modification of dopamine release by ischemia. At 100 nm, the antagonist elicited a slight ceiling effect on decreases in glutamate release by ischemia and protected neurons from cell death. Glutamate was released concentration-dependently by intrastriatal perfusion of 0.3,1 mm DOPA and stereoselectively by 0.6 mm DOPA. The antagonist elicited no hypothermia during and after ischemia. Endogenously released DOPA is an upstream causal factor for glutamate release and resultant delayed neuronal cell death by brain ischemia in rat striata. DOPA antagonist has a neuroprotective action. [source] 6-Formylpterin protects retinal neurons from transient ischemia,reperfusion injury in rats: A morphological and immunohistochemical studyNEUROPATHOLOGY, Issue 3 2003Taisaku Funakoshi Neuroprotective effects of 6-formylpterin (6FP) on transient retinal ischemia,reperfusion injury were evaluated in rats by means of counting the number of retinal ganglion cells, measuring the thicknesses of the inner plexiform and inner nuclear layers, and by immunohistochemical detection of apoptotic cells in the retina. Sixty-one Sprague,Dawley rats (12 weeks, male, 295,330 g) were subjected to transient retinal ischemia,reperfusion by elevated intra-ocular pressure (80 mmHg for 60 min). Intraperitoneal injection of 6FP (3.8 mg/kg) was performed before or after ischemia. The retina was histologically better preserved in rats with 6FP treatment than without 6FP treatment. 6FP showed more strong neuroprotective effects when it was administered before ischemia. The number of single-stranded DNA-positive cells in the retina also decreased remarkably in rats with 6FP treatment, especially when administered before ischemia. These results suggest that 6FP protects retinal neurons from transient ischemia,reperfusion injury, at least in part by inhibiting apoptotic cell death. [source] Age-related changes of cornu ammonis 1 pyramidal neurons in gerbil transient ischemiaNEUROPATHOLOGY, Issue 3 2000Chiharu Tamagaki This study reports that postischemic apoptotic cell death of the hippocampal cornu ammonis (CA) 1 neurons is delayed in aged gerbils. Age-related changes in the process of CA1 neuronal death following transient ischemia was studied. Two groups of Mongolian gerbils were used in this study, which compared adult (4-month-old) and aged (24-month-old) animals by hematoxylin,eosin stain, in situ nick-end labeling (TUNEL method) and electron microscopy. In the process of neuronal death, neuronal loss of the aged group was histologically less severe than that of the adult group. TUNEL-positive cells were found on days 3,5 after ischemia in the adult group, while they were still found on day 7 in the aged group. The apoptotic process of the aged group was delayed compared to the adult group. Furthermore, lipofuscin was ultrastructurally observed inside the apoptotic body 5 days after ischemia in CA1 pyramidal neurons of the aged group. It is likely that colocalization of lysosomal enzyme cathepsin D with lipofuscin might be associated with the age-related alteration of lysosomal system in the neurons. Altogether these data suggest that age-related lysosomal changes might affect the apoptotic cascade process in postischernic CA1 neurons. [source] Alterations in inorganic phosphate in mouse hindlimb muscles during limb disuse,NMR IN BIOMEDICINE, Issue 2 2008Neeti Pathare Abstract Muscle disuse induces a wide array of structural, biochemical, and neural adaptations in skeletal muscle, which can affect its function. We recently demonstrated in patients with an orthopedic injury that cast immobilization alters the resting Pi content of skeletal muscle, which may contribute to loss of specific force. The goal of this study was to determine the direct effect of disuse on the basal phosphate content in skeletal muscle in an animal model, avoiding the confounding effects of injury/surgery. 31P and 1H MRS data were acquired from the gastrocnemius muscle of young adult mice (C57BL6 female, n,=,8), at rest and during a reversible ischemia experiment, before and after 2 weeks of cast immobilization. Cast immobilization resulted in an increase in resting Pi content (75%; p,<,0.001) and the Pi to phosphocreatine (PCr) ratio (Pi/PCr; 80%, p,<,0.001). The resting concentrations of ATP, PCr and total creatine (PCr,+,creatine) and the intracellular pH were not significantly different after immobilization. During ischemia (30,min), PCr concentrations decreased to 54,±,2% and 52,±,6% of the resting values in pre-immobilized and immobilized muscles, respectively, but there were no detectable differences in the rates of Pi increase or PCr depletion (0.55,±,0.01,mM min,1 and 0.52,±,0.03,mM min,1 before and after immobilization, respectively; p,=,0.78). At the end of ischemia, immobilized muscles had a twofold higher phosphorylation potential ([ADP][Pi]/[ATP]) and intracellular buffering capacity (3.38,±,0.54 slykes vs 6.18,±,0.57 slykes). However, the rate of PCr resynthesis (kPCr) after ischemia, a measure of in vivo mitochondrial function, was significantly lower in the immobilized muscles (0.31,±,0.04,min,1) than in pre-immobilized muscles (0.43,±,0.04,min,1). In conclusion, our findings indicate that 2 weeks of cast immobilization, independent of injury-related alterations, leads to a significant increase in the resting Pi content of mouse skeletal muscle. The increase in Pi with muscle disuse has a significant effect on the cytosolic phosphorylation potential during transient ischemia and increases the intracellular buffering capacity of skeletal muscle. Copyright © 2007 John Wiley & Sons, Ltd. [source] In-vivo visualization of phagocytotic cells in rat brains after transient ischemia by USPIONMR IN BIOMEDICINE, Issue 4 2002M. Rausch Abstract Cerebral ischemia provokes tissue damage by two major patho-physiological mechanisms. Direct cell necrosis is induced by diminished access of neurons and glia to essential nutrients such as glucose and oxygen leading to energy failure. A second factor of cellular loss is related to the activation of immune-competent cells within and around the primary infarct. While granulocytes and presumably monocytes are linked to the no-reflow phenomenon, activated microglia cells and monocytes can release cytotoxic substrates, which cause delayed cell death. As a consequence the infarct volume will increase, despite restoration of cerebral perfusion. In the past, visualization of immune competent cells was only possible by histological analysis of post-mortem tissue. However, contrast agents based on small particles of iron oxide are known to accumulate in organs rich in cells with phagocytotic function. These particles can be tracked in vivo by MRI methods based on their relaxation properties. In the present study, the spatio-temporal distribution of USPIO particles was monitored in a rat model of transient cerebral infarction using T1 - and T2 -weighted MRI sequences. USPIO were detected in vessels at 24,h after administration. At later time points specific accumulation of USPIO was observed within the infarcted hemisphere, with maximal signal enhancement on day 2. Their detectability based on T1 -contrast disappeared between day 4 and day 7. Immuno-histochemically (IHC) stains confirmed the presence of macrophages, presumably blood-derived monocytes within areas of T1 signal enhancement. Direct visualization of iron-burdened macrophages by IHC was only possible later than day 3 after occlusion. Copyright © 2002 John Wiley & Sons, Ltd. [source] Pacemaker Lead Extraction with the Needle's Eye Snare for Countertraction via a Femoral ApproachPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 7 2002DIDIER KLUG KLUG, D., et al.: Pacemaker Lead Extraction with the Needle's Eye Snare for Countertraction via a Femoral Approach. Femoral approach pacemaker lead extraction is described as a safe and efficacious procedure. When the lead can not be removed from its myocardial insertion, the "Needle's eye snare" has become available, and it allows a femoral approach traction associated with a countertraction . Between May 1998 and May 2000, 222 lead extraction procedures were performed in 99 patients using the femoral approach. This article reports the results of the 70 lead extractions requiring the use of the Needle's eye snare for femoral approach countertraction in 39 patients with a total of 82 leads. The indications were infection, accufix leads and lead dysfunction in 56, 1 and 6 leads, respectively. The age of the leads was 113 ± 56 months. Sixty-one (87.2%) leads were successfully extracted, the extraction was incomplete in 3 (4.3%) cases and failed in 6 (8.5%) cases. The failures were due to leads totally excluded from the venous flow for four leads, the impossibility of advancing the 16 Fr long sheath through the right and left iliac veins for one lead and one traction induced a nontolerated ventricular arrhythmia. In these cases, an extraction by a simple upper traction had been attempted in another center several months before. The complications included two deaths and one transient ischemia of the right inferior limb. Despite the selection of a series of leads for which an extraction by a simple traction on the proximal end of the lead was impossible or unsuccessful, femoral countertraction seems to be a safe and efficacious procedure. The failure of this technique occurred in patients with damaged leads due to a previous extraction procedure performed in centers with limited experience in lead extraction. [source] Recombinant C1 inhibitor in brain ischemic injury,ANNALS OF NEUROLOGY, Issue 3 2009Raffaella Gesuete BD Objective C1 inhibitor (C1-INH) is an endogenous inhibitor of complement and kinin systems. We have explored the efficacy and the therapeutic window of the recently available human recombinant (rh) C1-INH on ischemic brain injury and investigated its mechanism of action in comparison with that of plasma-derived (pd) C1-INH. Methods rhC1-INH was administered intravenously to C57Bl/6 mice undergoing transient or permanent ischemia, and its protective effects were evaluated by measuring infarct volume and neurodegeneration. The binding profiles of rhC1-INH and pdC1-INH were assessed in vitro using surface plasmon resonance. Their localization in the ischemic brain tissue was determined by immunohistochemistry and confocal analysis. The functional consequences of rhC1-INH and pdC1-INH administration on complement activation were analyzed by enzyme-linked immunosorbent assay on plasma samples. Results rhC1-INH markedly reduced cerebral damage when administered up to 18 hours after transient ischemia and up to 6 hours after permanent ischemia, thus showing a surprisingly wide therapeutic window. In vitro rhC1-INH bound mannose-binding lectin (MBL), a key protein in the lectin complement pathway, with high affinity, whereas pdC1-INH, which has a different glycosylation pattern, did not. In the ischemic brain, rhC1-INH was confined to cerebral vessels, where it colocalized with MBL, whereas pdC1-INH diffused into the brain parenchyma. In addition, rhC1-INH was more active than pdC1-INH in inhibiting MBL-induced complement activation. Interpretation rhC1-INH showed a surprisingly wider time window of efficacy compared with the corresponding plasmatic protein. We propose that the superiority of rhC1-INH is due to its selective binding to MBL, which emerged as a novel target for stroke treatment. Ann Neurol 2009;66:332,342 [source] Characterizing the diffusion/perfusion mismatch in experimental focal cerebral ischemiaANNALS OF NEUROLOGY, Issue 2 2004Xiangjun Meng MD Diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) can rapidly detect lesions in acute ischemic stroke patients. The PWI volume is typically substantially larger than the DWI volume shortly after onset, that is, a diffusion/ perfusion mismatch. The aims of this study were to follow the evolution of the diffusion/ perfusion mismatch in permanent and 60- minute temporary focal experimental ischemia models in Sprague-Dawley rats using the intraluminal middle cerebral artery occlusion (MCAO) method. DWI and arterial spin-labeled PWI were performed at 30, 60, 90, 120, and 180 minutes after occlusion and lesion volumes (mm3) calculated At 24 hours after MCAO, and infarct volume was determined using triphenyltetrazolium chloride staining. In the permanent MCAO group, the lesion volume on the ADC maps was significantly smaller than that on the cerebral blood flow maps through the first 60 minutes after MCAO; but not after 90 minutes of occlusion. With 60 minutes of transient ischemia, the diffusion/perfusion mismatch was similar, but after reperfusion, the lesion volumes on ADC and cerebral blood flow maps became much smaller. There was a significant difference in 24- hour infarct volumes between the permanent and temporary occlusion groups. [source] Observer Variability and Optimal Criteria of Transient Ischemia During ST Monitoring with Continuous 12-lead ECGANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2002Ph.D., Tomas Jernberg M.D. Background: ST monitoring with continuous 12-lead ECG is a well-established method in patients with unstable coronary artery disease (CAD). However, the method lacks documentation on optimal criteria for episodes of transient ischemia and on observer variability. Methods: Observer variability was evaluated in 24-hour recordings from 100 patients with unstable CAD with monitoring in the coronary care unit. Influence on ST changes by variations in body position were evaluated by monitoring 50 patients in different body positions. Different criteria of transient ischemia and their predictive importance were evaluated in 630 patients with unstable CAD who underwent 12 hours of monitoring and thereafter were followed for 1 to 13 months. Two sets of criteria were tested: (1) ST deviation , 0.1 mV for at least 1 minute, and (2) ST depression , 0.05 mV or elevation , 0.1 mV for at least 1 minute. Results: When the first set of criteria were used, the interobserver agreement was good (kappa = 0.72) and 8 (16%) had significant ST changes in at least one body position. Out of 100 patients with symptoms suggestive of unstable CAD and such ischemia, 24 (24%) had a cardiac event during follow-up. When the second set of criteria were used, the interobserver agreement was poor (kappa = 0.32) and 21(42%) had significant ST changes in at least one body position. Patients fulfilling the second but not the first set of criteria did not have a higher risk of cardiac event than those without transient ischemia (5.3 vs 4.3%). Conclusions: During 12-lead ECG monitoring, transient ischemic episodes should be defined as ST deviations , 0.1 mV for at least 1 minute, based on a low observer variability, minor problems with postural ST changes and an important predictive value. A.N.E. 2002;7(3):181,190 [source] Lack of Impact of Myocardial Ischemia on the Signal-Averaged ECG Assessment by Time-Domain AnalysisANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2002Michael A. E. Schneider M.D. Background: Late potentials represent an arrhythmogenic substrate in chronically infarcted myocardium. It is hypothesized that acute transient ischemia enhances anisotropic electrical ventricular activation and facilitates reentry mechanisms. Study aim was the prospective assessment of the impact of dipyridamole-induced myocardial ischemia on the signal-averaged ECG. Methods: Dipyridamole stress thallium-201 SPECT imaging was utilized to avoid noise contamination of the signal-averaged ECG from exercise and to document evidence and localization of myocardial ischemia or persistent perfusion defects in 68 patients with suspected coronary artery disease. Before and during dipyridamole-induced vasodilatation serial signal-averaged ECG was performed to evaluate the influence of transient ischemia on the occurrence of late potentials. Results: There was a significant difference between heart rate at rest and heart rate under dipyridamole influence in patients with inducible ischemia (70 ± 13 vs. 87 ± 13; P < 0.0001) in contrast to patients without dipyridamole-induced ischemia (74 ± 20 vs. 80 ± 16; n.s.). The number of averaged beats and achieved noise level was comparable between both groups. Thirty-three of 68 patients (49%) revealed dipyridamole-induced ischemia; however, no changes of the SAECG parameters, such as QRS, RMS, LAS at 25,250 and 40,250 Hz bandpass filtering in the leads X, Y, Z and vector magnitude, respectively, were observed as a result of ischemia. Conclusion: These results suggest that transient myocardial ischemia does not affect the signal-averaged ECG. Clinically, the signal-averaged ECG analysis seems not to be helpful in identifying patients with silent ischemia. A.N.E. 2002;7(3):191,197 [source] The Transcriptional Coactivator p300 Plays a Critical Role in the Hypertrophic and Protective Pathways Induced by Phenylephrine in Cardiac Cells but Is Specific to the Hypertrophic Effect of UrocortinCHEMBIOCHEM, Issue 1 2005Sean M. Davidson Dr. Abstract Anacardic acid is an alkylsalicylic acid obtained from cashew-nut-shell liquid, and is a potent inhibitor of p300 histone acetyl-transferase (HAT) activity. We have used anacardic acid to prevent the induction of hypertrophy in isolated neonatal rat cardiomyocytes. Hypertrophy was detected as an increase in cell size, the rearrangement of sarcomeres into a striated pattern, and the induction of embryonic genes ,-MHC and ANF. p300 inhibition was equally effective at preventing hypertrophy whether it was induced by treatment with the ,1-adrenergic agonist, phenylephrine, or by treatment with urocortin, a member of the corticotrophin-releasing-factor family, which stimulates specific G protein-coupled receptors. Spiruchostatin A is a natural-product inhibitor of histone deacetylases (HDAC) similar to the depsipeptide FK228 molecule. We have recently synthesized spiruchostatin A and now show that, although HDACs act in opposition to HATs, spiruchostatin A has the same effect as anacardic acid, that is, it prevents the induction of hypertrophy in response to phenylephrine or urocortin. Pretreatment with either phenylephrine or urocortin reduced the extent of death observed after the exposure of isolated cardiomyocytes to simulated ischaemia and reoxygenation. Inhibition of p300 or HDAC activity eliminated the protection conferred by phenylephrine; however, it did not affect the protection conferred by urocortin. Therefore, it might eventually be possible to use chemical inhibitors such as these in a therapeutic setting to dissociate the protective effect and hypertrophic effect of urocortin, enhancing the survival of cardiomyocytes exposed to transient ischemia, while inhibiting the hypertrophic pathway that would otherwise be induced concurrently. [source] Epidemiology and stratification of risk for sudden cardiac deathCLINICAL CARDIOLOGY, Issue S1 2005Philip J. Podrid M.D. Abstract Sudden cardiac death (SCD) is a major cause of mortality in the United States. Approximately 65% of cases of SCD occur in patients with underlying acute or chronic ischemic heart disease. The incidence of SCD increases 2- to 4-fold in the presence of coronary disease and 6- to 10-fold in the presence of structural heart disease. Ventricular fibrillation (VF) precipitated by ventricular tachycardia (VT) is a common mechanism of cardiac arrest leading to SCD. Triggers for SCD include electrolyte disturbances, heart failure, and transient ischemia. Although a large percentage of patients with out-of-hospital SCD do not survive, successful resuscitation to hospitalization has improved in recent years. One of the challenges for preventing SCD lies in identifying individuals at highest risk for SCD within a lower-risk population. The progression from conventional risk factors of coronary artery disease to arrhythmogenesis and SCD can be represented as a cascade of changes associated with levels of increasing risk. At the first level is atherogenesis, followed by changes in atherosclerotic plaque anatomy, which may be mediated by inflammatory processes. Disruption of active plaque formed during a transitional state initiates the thrombotic cascade and acute occlusion, after which acute changes in myocardial electrophysiology become the immediate trigger for arrhythmogenesis and SCD. Each level of the cascade offers different opportunities for risk prediction. Among the classes of risk predictors are clinical markers, such as ECG measures and ejection fraction. Transient risk markers, such as inflammatory markers, are potentially useful for identifying triggers for SCD. In the future, genetic profiling is expected to allow better assessment of individual risks for SCD. [source] New parameters in the interpretation of exercise testing in women: QTC dispersion and QT dispersion ratio differenceCLINICAL CARDIOLOGY, Issue 4 2002Kurtulu, Özdemr M.D. Abstract Background: It has been reported that the increase of QT dispersion (QTD) that occurs due to increased inhomogeneity of the ventricular repolarization because of transient ischemia obtained by standard 12-lead electrocardiogram (ECG), the changes during exercise, and the differences between exercise and rest increase the accuracy of exercise test in the diagnosis of coronary artery disease (CAD). Hypothesis: This study was designed to investigate the value of QTD parameters, which are reported to increase the diagnostic accuracy of exercise test in women. Methods: Ninety-seven women who had undergone coronary angiography and exercise test were evaluated for diagnosis of chest pain. QT dispersion was calculated using the measurements of the highest and lowest values of QT interval obtained by ECG during peak exercise. The QTc using Bazett's equation, and the QTD ratio (QTDR) using QT/RR were calculated, and QTcD and QTD ratios were obtained. The difference between QTcD and QTDR was determined by extracting the rest values from the exercise values. Results: The groups with normal coronaries (n = 48), single-vessel CAD (n= 24), and multivessel CAD (n= 25) were compared. The obtained QTD parameters at peak exercise and their differences between exercise and rest were found to be significantly increased in patients with CAD (p<0.001). Furthermore, these parameters were found to be higher in the patients with multivessel CAD than in those with single-vessel disease (p < 0.05). With the parameters QTcD > 60 ms and QTDR > 10%, greater sensitivity and specificity were obtained compared with ST-segment depression. The highest diagnostic accuracy was obtained with the QTD parameters calculated from the differences between rest and exercise values. The diagnostic accuracy of the difference of QTcD > 15 ms and the difference of QTDR > 5% was relatively higher than the other parameters (sensitivity, specificity, and negative and positive predictor values are 84,88,84, 87% and 84, 96, 85, 95%, respectively). Conclusion: The use of QTD parameters as variables of ECG, which is easily obtainable in the evaluation of exercise ECG in women, increases the diagnostic accuracy of the exercise test. In addition, the evaluation of QTD variables may provide information about the incidence of CAD. [source] | |||||||||||||